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Cadmium Toxicity TSDR_______________________________ June 1990 Case Studies in Environmental Medicine Cadmium Toxicity -S»tucnart4He*cfal ALERT . \AS\ Prevention is the key to managing cadmium exposure; no effective treatment for '---- ------cadmium toxicity exists. Ef Nutritional deficiencies can increase the risk of cadmium toxicity. ET Cadmium affects primarily the renal and skeletal systems. This monograph is one in a series of self-instructional publications designed to increase the primary care provider's knowledge of hazardous substances in the environment and to aid in the evaluation of potentially exposed patients. See page 21 for further information about continuing medical education credits and continuing education units. Guest Contributor: Emily E. Grum, MD Guest Editor: Eddy A. Bresnitz, MD, MS Peer Reviewers:Charles Becker, MD; Jonathan Borak, MD; Joseph Cannella, MD; Bernard Goldstein, MD; Alan Hall, MD; Richard J. Jackson, MD, MPH; Jonathan Rodnick, MD; LAND Robert Wheater, MS; Brian Wummer, MD WA 30 C337 n o . 10 1990 U.S. DEPARTMENT OF HEALTH & HUMAN SERVICES Public Health Service Agency for Toxic Substances and Disease Registry V A lan d WA30 C337 no.10 1990 — A r s o n _____________________ _Dept, of Health & Human W Services, Public Health » Cadmium toxicity How to use this issue... This issue begins with a composite case study that describes a realistic encounter with a patient. This description is followed by a pretest. The case study is further developed through Challenge questions at the end of each section. To fully benefit from this monograph, readers are urged to answer each question when it is presented. (Answers to the Pretest and Challenge questions are found on pages 18-19.) The monograph ends with a posttest, which can be submitted to ATSDR for continuing medical education (CME) credit or continuing education units (CEU). See page 21 for further instructions on how to receive these credits. The objectives of this monograph on cadmium are to help you: □ Explain why cadmium is a chronic health hazard □ Describe the known factors contributing to cadmium poisoning □ Identify potential environmental or occupational sources of exposure to cadmium □ Identify evaluation and treatment protocols for persons exposed to cadmium □ List sources of information on cadmium Contents Case Study............................................... 1 Pretest...................................................... 1 Exposure Pathways..................................2 Who's at Risk............................................ 3 Biologic Fate............................................. 5 Physiologic Effects....................................7 Clinical Evaluation..................................10 Treatment and Management ................. 14 Standards and Regulations ................... 15 Suggested Reading L ist.........................17 Answers to Questions.............................18 Sources of Information............................20 Posttest and Credits...............................21 This issue is prepared with the assistance of those who share a common concern for physician education, public health, and the environment, including the following organizations: American Academy of Family Physicians (AAFP), American Academy of Pediatrics (AAP), American College of Emergency Physicians (ACEP), American College of Occupational and Environmental Medicine (ACOEM), American Medical Association (AMA), Associa­ tion of State and Territorial Health Officials (ASTHO), and the Society of Teachers of Family Medicine (STFM). Final responsibility for the contents and views expressed in this monograph resides with ATSDR. Agency for Toxic Substances and Disease Registry Project Officers: Max Lum, EdD, and Donna Orti, MS Prepared by DeLima Associates, San Rafael, California, under Contract No. 205-88-0636 Case Study Low back pain and waddling gait in a 60-year-old woman A 60-year-old woman comes to your office with complaints of low back pain, which is causing progressive difficulty in walking. The pain has gradually increased since the onset of menopause 5 years ago. This discomfort is especially noticeable after prolonged sitting. Social history reveals that the patient has been a housewife since her marriage 38 years ago. Her husband, who is in good health, owns and operates a small retail shop in their home. The patient has been making jewelry for sale in her husband’s shop and as a hobby for about 35 years. They have two adult sons who are in good health. The patient denies a personal or family history of kidney disease, hypertension, diabetes mellitus, or cardiovascular disease; she also denies history of back trauma or weight loss. She has smoked one to two packs of cigarettes a day for the past 40 years. She does not take estrogens, calcium supplements, vitamins, or other medications. On examination you find a thin female with a slightly stooped posture and a waddling gait. Blood pressure is 120/70. Her teeth have a yellow discoloration above the crown, and her fingernails are stained with nicotine. She is anosmic on cranial nerve examination. Results of cardiovascular and abdominal examina­ tion are normal. The lower lumbar spine is tender to percussion, but the patient does not complain of pain on straight leg raising. Her deep tendon reflexes are intact, and the remainder of the physical examination, including neurologic testing, is normal. Sensation and strength are normal in legs and feet. Range of motion is normal in hips and knees. Initial laboratory data include a urinalysis showing 3+ proteinuria and glycosuria. BUN, creatinine, and albumin levels are normal. Roentgenograms of the pelvis and lumbosacral spine reveal pseudofractures and other evidence of severe osteomalacia and mild osteoporosis. There are no osteolytic or osteoblastic lesions. (a) What should be included on the patient’s problem list? (b) What additional information would be helpful in diagnosing this woman’s condition? (c) What further tests, if any, would you recommend? (d) What treatment would be appropriate for this patient? Answers to the Pretest are included in Challenge answers (6) through (9) on page 19. 1 = A tsdr________________ Exposure Pathways □ in the general population, Pure cadmium is a silver-white, lustrous metal, but cadmium in exposure to cadmium this form is not common in the environment. It is most often occurs primarily by eating encountered in the earth’s crust combined with chlorine (cad­ crops grown in contami­ mium chloride), oxygen (cadmium oxide), and sulfur (cadmium nated soil and seafood. sulfide). Cadmium oxide also exists as small particles in air □ Airborne cadmium sources (fume), the result of smelting, soldering, or other high-tempera- include combustion of ture industrial processes. Most cadmium used in the United fossil fuels, incineration States is obtained as a byproduct of the smelting of zinc, lead, of municipal waste, and or copper ores. Cadmium is used mainly in metal plating; in smelter emissions. producing pigments, batteries, and plastics; and as a neutron absorbant in nuclear reactors. Foods are the most important source of cadmium exposure for the general population. Low levels of cadmium are found in basic foodstuffs, especially grains, cereals, and leafy vege­ tables, which readily absorb naturally occurring cadmium or cadmium in soil contaminated by sewage sludge, fertilizers, and polluted groundwater. In 1946, the inhabitants of the Jintzu River basin in Japan were afflicted with a disease characterized by pain and bone fractures (called itai-itai or ouch-ouch dis­ ease), which was caused by high levels of cadmium in water and rice, the result of using water contaminated by discharges from a local zinc-mining operation. Cadmium bioaccumulates in the food chain; consequently, ingestion of animal internal organs, such as liver and kidneys, and some types of fish and shellfish may result in increased exposure. The greatest sources of airborne cadmium are burning fossil fuels such as coal or oil, and incineration of municipal waste such as plastics and nickel-cadmium batteries. Cadmium may also escape into the air from zinc, lead, or copper smelters, and from iron and steel production facilities. Like most plants, tobacco contains cadmium, which is inhaled in cigarette smoke. Cadmium concentrations in drinking water supplies are typically less than 1 microgram per liter (^ig/L) or 1 part per billion (ppb). Groundwater seldom contains high levels of cadmium unless it is contaminated by mining or industrial wastewater, or seepage from hazardous waste sites. Soft or acidic water tends to dis­ solve cadmium and lead from water lines; cadmium levels are increased in water stagnating in household pipes. These sources have not caused clinical cadmium poisoning, but even low levels of contamination presumably contribute to the body’s accumula­ tion of cadmium. 2 Cadmium Toxicity Cadmium is a component of chuifong tokwan, pharmaceutical a compound manufactured in Asia and sold illegally in the United States as a “miracle herb.” Some artists’ paints contain a yellow pigment made from cadmium sulfide. Cadmium at one time was \ a leachable component of the alloy used in ice cube trays. Who's at Risk Background levels of cadmium in food, water, and ambient air □ Workers in industries pro­ are not a health concern for the general North American popu­ ducing or using cadmium lation. Typical dietary intake is about 30 micrograms of cadmium have the greatest potential per day (30 (i.g/day), a rate roughly 10 times lower than
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